肠内补充维生素E可抑制细胞因子对内毒素的反应。

Enteral vitamin E supplementation inhibits the cytokine response to endotoxin.

作者信息

Bulger E M, Helton W S, Clinton C M, Roque R P, Garcia I, Maier R V

机构信息

Department of Surgery, University of Washington, Seattle 98195, USA.

出版信息

Arch Surg. 1997 Dec;132(12):1337-41. doi: 10.1001/archsurg.1997.01430360083015.

DOI:10.1001/archsurg.1997.01430360083015

PMID:9403540

Abstract

OBJECTIVE

To evaluate the effect of short-term, high-dose enteral supplementation of 3 different vitamin E derivatives: free alpha-tocopherol (VE), alpha-tocopherol succinate (VES), and alpha-tocopherol acetate (VEA) on macrophage and monocyte activation.

DESIGN

Sprague-Dawley rats (weight, 150-200 g) were assigned to 1 of 5 experimental groups: saline (control), ethanol (control), VES (100 mg/kg), VEA (100 mg/kg), or VE (100 mg/kg). Rats underwent oral gavage once per day for 5 days with 0.5 mL of their assigned solution. All vitamin E derivatives were diluted in 75% ethanol. Rats were then killed and whole-blood and peritoneal macrophages were harvested and stimulated with lipopolysaccharide (10 microg/mL) in vitro. Tumor necrosis factor (TNF) production was measured by enzyme-linked immunosorbent assay. Additional serum samples were analyzed for alpha-tocopherol concentration by high-performance lipid chromatography.

RESULTS

Whole-blood TNF production was maximal in the control groups after 3 hours of incubation and began to decline by 6 hours. Supplementation with all 3 vitamin E derivatives resulted in suppression of lipopolysaccharide-induced TNF production at both time points when compared with both ethanol and saline controls (P<.05, analysis of variance [ANOVA]). All 3 vitamin E derivatives also resulted in significant inhibition of lipopolysaccharide-induced TNF production by peritoneal macrophages when compared with their ethanol-carrier control but not with the saline control (P<.05, ANOVA). The degree of TNF suppression correlated directly with serum alpha-tocopherol levels.

CONCLUSIONS

Our data demonstrate that a short-term, high-dose enteral supplementation of vitamin E can modulate the monocyte and macrophage response to endotoxin. These data, along with other animal studies showing a protective effect of vitamin E treatment in sepsis and ischemia-reperfusion injury, suggest a potential role for vitamin E supplementation in patients at risk of the systemic inflammatory response syndrome.

摘要

目的

评估短期、高剂量肠内补充3种不同维生素E衍生物：游离α-生育酚（VE）、α-生育酚琥珀酸酯（VES）和α-生育酚乙酸酯（VEA）对巨噬细胞和单核细胞激活的影响。

设计

将Sprague-Dawley大鼠（体重150 - 200 g）分为5个实验组之一：生理盐水（对照组）、乙醇（对照组）、VES（100 mg/kg）、VEA（100 mg/kg）或VE（100 mg/kg）。大鼠每天经口灌胃1次，连续5天，给予0.5 mL指定溶液。所有维生素E衍生物均用75%乙醇稀释。然后处死大鼠，收集全血和腹腔巨噬细胞，并在体外用脂多糖（10 μg/mL）刺激。通过酶联免疫吸附测定法测量肿瘤坏死因子（TNF）的产生。通过高效脂质色谱法分析额外的血清样本中的α-生育酚浓度。

结果

孵育3小时后，对照组全血TNF产生量最大，6小时后开始下降。与乙醇和生理盐水对照组相比，补充所有3种维生素E衍生物均导致在两个时间点脂多糖诱导的TNF产生受到抑制（P<0.05，方差分析[ANOVA]）。与乙醇载体对照组相比，所有3种维生素E衍生物还导致腹腔巨噬细胞脂多糖诱导的TNF产生受到显著抑制，但与生理盐水对照组相比无显著差异（P<0.05，ANOVA）。TNF抑制程度与血清α-生育酚水平直接相关。